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In vivo, the data of established transgenic animals showed that mice with lncHR1 expression had less hepatic expression of SREBP-1c, FAS, Acetyl-CoA carboxylase alpha (ACCalpha), and less he (show FASN Proteins)patic and plasma TG after being fed a high-fat diet.
dysregulation of SIRT1 (show SIRT1 Proteins)-AMPK (show PRKAA1 Proteins)-SREBP and stimulation of NLRP3 (show NLRP3 Proteins) inflammasome may contribute to vascular lipid deposition and inflammation in atherosclerosis
Polymorphisms of the ACACA and SREBF1 genes are promising markers for pig carcass and performance traits.
IL-4 induced activation of Akt/SREBP-1/lipid biosynthesis in EC, resulting in protection against membrane attack complex and melittin, in association with mitochondrial protection.
Basal transcription and supra-additive stimulation of porcine LDLR gene transcription by LH and insulin in granulosa-luteal cells require SREBP-1a and Sp1/Sp3-binding elements.
Results of associated analysis show that the polymorphism of ADD1 gene was associated traits of Intramuscular fat content (IMF (show MDFI Proteins)) and back fat thickness (BF).
SREBF1 might play an important role in regulation of muscle fat deposition during postnatal growth of pigs.
SREBP1a activated while C/EBP (show CEBPA Proteins) factors downregulated the activity of the SCD1 (show SCD Proteins) promoter.
These results suggest that increased expression of hepatic CD36 (show CD36 Proteins) and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation.
Hepatic SREBP-1c-mediated lipid synthesis and the NF-kappaB (show NFKB1 Proteins) inflammatory pathway were both overinduced in cows with fatty liver.
SREBP1 was found to be a key positive regulator of milk fat synthesis and was shown to be regulated by stearic acid and serum.
data suggest that low SREBP-1c expression can decrease lipid synthesis, increase lipid oxidation, and decrease the TG and VLDL content in bovine hepatocytes
84-bp indel in intron 5 was significantly associated with palmitoleic acid, stearic acid, saturated fatty acids, triglycerides and the C16 index in Simmental bulls.
genetic polymorphisms in sterol regulatory element binding transcription factor 1 (SREBF1)can be used to develop genetic tools for the selection of animals producing milk with healthier fatty acid composition
The results of this study demonstrated the existence of the polymorphisms in the SCD1 (show SCD Proteins) and SREBP-1 genes in the population of Fleckvieh cattle and their associations with the concentrations of several muscle fat and subscutaneous fat fatty acids.
These results provide detailed genetic information for the SREBP1 signalling pathway and SCD (show SCD Proteins) that can be used to change milk fat composition by marker-assisted breeding.
The SREBP1-9 SNP showed a significant effect on marbling score, monounsaturated fatty acids and C18 (show BBS9 Proteins):1n-9 in the muscle fat of commercial Korean cattle.
the ability of Pu-erh (show ERH Proteins) tea in promoting inhibition of food uptake and the biosynthesis of fat via SBP-1 and SCD (show SCD Proteins), thereby reducing fat storage.
SBP-1/SREBP-1 is part of a conserved feedback loop responding to phosphatidylcholine (show SGMS1 Proteins) levels to regulate expression of one-carbon cycle biogenesis genes and ensure adequate S-adenosylmethionine levels for phosphatidylcholine (show SGMS1 Proteins) production.
elo-5 and elo-6 may be transcriptional targets of LPD (show ACSBG1 Proteins)-1
both SBP-1 and MDT-15 control transcription of genes governing desaturation of stearic acid to oleic acid
Essential role of sbp-1 activation in oxygen deprivation induced lipid accumulation and increase in body width/length ratio in Caenorhabditis elegans.
Variants in the TOM1L2/SREBF1 (show TOM1L2 Proteins) locus exert opposing effects of total-body lean mass (TB-LM) and total-body less head bone mineral density (TBLH-BMD (show BEST1 Proteins)) .
Date indicate that sterol regulatory element-binding proteins Srebp1 and Srebp2 (show SREBF2 Proteins) are essential for the metabolic reprogramming of NK cells and for the attainment of elevated glycolysis and oxidative phosphorylation.
Study identified a novel human specific lncRNA, lncHR1, as a negative regulator of SREBP-1c expression. Overexpression of lncHR1 inhibited expression of SREBP-1c and fatty acid synthase (FAS (show FASN Proteins)) and then repressed oleic acid-induced hepatic cell triglyceride (TG) and lipid droplet (LD) accumulation.
Glucose adsorption to chitosan membranes increases proliferation of human chondrocytes via mammalian target of rapamycin (show FRAP1 Proteins) complex 1 and sterol regulatory element-binding protein-1 signaling.
miR (show MLXIP Proteins)-185 negatively regulates the differentiation of 3T3-L1 cells by targeting SREBP-1
The authors further demonstrated that the upregulation of sterol regulatory element-binding protein (show CNBP Proteins) (SREBP)-1c by activation of the Akt (show AKT1 Proteins) and p70S6K (show RPS6KB1 Proteins) pathways is critical for high-glucose-treated Porphyromonas gingivalis-induced NLRP3 (show NLRP3 Proteins) expression.
Results show that PPARalpha (show PPARA Proteins) is downregulated and SREBP-1c is upregulated in steatosis L-02 cells. These changes increase lipid synthesis and reduce lipid disposal, which ultimately lead to hepatic steatosis.
SREBP-1 and SREBP-2 mRNA expression levels were measured in EAT from 49 patients with CAD (26 with diabetes) and 23 controls without CAD or diabetes.SREBP expression was associated as cardiovascular risk factor for the severity of CAD and the poor lipid control.
The involvement of SREBP-1c in FASN (show FASN Proteins) promoter histone modification.
the mitotic phosphorylation and stabilization of nuclear SREBP1 during cell division provides a link between lipid metabolism and cell proliferation.
The deletion of Srebf-2 (show SREBF2 Proteins) and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR (show NR1H3 Proteins) activity and SREBP-1c expression.
The fasting-induced (show C10orf10 Proteins) transcription factor KLF15, a key regulator of gluconeogenesis, forms a complex with LXR (show NR1H3 Proteins)/RXR, specifically on the Srebf1 (show TOM1L2 Proteins) promoter.
Exposure to a xenobiotic during early development induced persistent fat accumulation via hypomethylation of lipogenic genes. Moreover, increased Nrf2 (show NFE2L2 Proteins) recruitment to the Srebp-1c promoter in livers of BPA (show DST Proteins)-exposed mice was observed.
suggesting a specific effect of sterol regulatory element binding protein (show CNBP Proteins)-1c on neurosteroidogenesis
Transforming growth factor-beta activated kinase 1 (TAK1 (show MAP3K7 Proteins)) regulation of sterol-regulatory element-binding proteins (SREBPs) critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent hepatocellular carcinoma (HCC (show FAM126A Proteins)) development.
SREBP1 pathway plays an important role in hepatocellular carcinoma pathogenesis.
In hepatocytes, E4BP4 (show NFIL3 Proteins) interacts with nuclear SREBP-1c to preserve its acetylation, and subsequently protects it from ubiquitination-dependent degradation
SREBP1 also contributes to the resolution phase of TLR4 (show TLR4 Proteins)-induced gene activation by reprogramming macrophage lipid metabolism.
27OH is not an important regulator of Srebp- or LXR regulated genes under basal conditions in mouse liver
This gene encodes a transcription factor that binds to the sterol regulatory element-1 (SRE1), which is a decamer flanking the low density lipoprotein receptor gene and some genes involved in sterol biosynthesis. The protein is synthesized as a precursor that is attached to the nuclear membrane and endoplasmic reticulum. Following cleavage, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit the cleavage of the precursor, and the mature nuclear form is rapidly catabolized, thereby reducing transcription. The protein is a member of the basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor family. This gene is located within the Smith-Magenis syndrome region on chromosome 17. Two transcript variants encoding different isoforms have been found for this gene.
, class D basic helix-loop-helix protein 1
, sterol regulatory element-binding protein 1
, adipocyte determination- and differentiation-dependent factor 1
, sterol regulatory element binding protein 1
, adipocyte determination and differentiation-dependent factor 1
, sterol regulatory binding transcription factor 1
, sterol regulatory element-binding transcription factor 1
, sterol regulatory element binding-protein 1
, sterol regulatory element binding transcription factor 1
, sterol response element binding protein 1
, similar to sterol regulatory element binding transcription factor 1 isoform b
, sterol regulatory element binding protein-1
, sterol regulatory element-binding protein 1-like
, Sterol regulatory element Binding Protein family member (sbp-1)
, Sterol regulatory element-binding transcription factor 1